Purpose of review
One of the major concerns in global health is the deteriorating control of dyslipidemia (DLD), which is a very strong modifiable risk factor for untoward cardiovascular disease (CVD) outcomes. It serves as a foundation for atherosclerotic lesions that can be destabilized by co-inflammatory processes leading to distal clot migration and other related CVD events. There are many misconceptions regarding the management of DLD. Many health sectors advocate for weight loss without a clear-cut target to achieve better CVD outcomes. There is growing evidence that exercise training compliance regardless of weight change is a more reliable indicator of favorable outcomes. This review is intended to understand the relationship between exercise training, lipoprotein readings, and with CVD and all-cause morbidity and mortality.
Aerobic exercise training (aET) and resistance exercise training (rET) increase cardiorespiratory fitness (CRF) and muscular strength (MusS), respectively. Regardless of weight loss, aET and rET are both known to independently reduce mortality possibly partly through improvement of lipid profiles. Of the two modes of exercise, rET has propensity for enhanced compliance because of its significant lipid and mortality-attenuating effect even with just brief exercise sessions. However, there are several studies showing that participation in both modes of exercise causes more pronounced improvements in DLD and CVD-related mortality compared with either mode of exercise training alone. In addition, Lipoprotein-a [Lp(a)] has been increasingly acknowledged to be atherogenic because of its LDL core. The close proximity of Lp(a) with macrophages triggers the development of atheromas, plaque formation, and growth. This causes a cascade of inflammatory processes that increase the development of ischemic CVD and calcific aortic valve stenosis. Although exercise training is known to reduce plasma LDL-C levels, it has no direct effect on Lp(a) levels as the latter lipoprotein is not influenced by motion nor exercise. Reviews of multiple studies lead us to infer that exercise training may potentially have an indirect impact on Lp(a) attenuation because of the ability of exercise training to inhibit Proprotein Convertase Subtisilin/Kexin type-9 (PCSK-9), as some studies using pharmacologic therapy with PCSK-9 inhibitors were able to show a concomitant decrease in Lp(a) levels.
It is clear that normal-to-overweight populations who are highly active have better CVD outcomes and lipid profiles than their sedentary counterparts, and those who were underweight and unfit fared much worse. This allows us to take a more precise approach in the management of DLD rather than plainly focusing on gross weight in patients. Exercise training certainly has beneficial impact on longevity owing to its advantageous effect on lipoprotein levels and particle size. As such, reputable health societies, such as the ESC, ACC, and AHA have prescribed the ideal exercise training regimen, which have noticeable similarities. Increasing the use of wearable devices may help improve our ability to prescribe, quantify, and precisely track physical activity in our continuing efforts to combat increasing morbidity related to unhealthy lifestyles and inactivity.